Evidence map›Paper›PMID 24210161›Full record

ArticleDrug and alcohol dependence2014

Juvenile exposure to ketamine causes delayed emergence of EEG abnormalities during adulthood in mice.

R E Featherstone, L R Nagy, C G Hahn, S J Siegel

Open access · greenAbstract read
In one paragraph

Article in Drug and alcohol dependence, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 15 citations in OpenAlex.

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  5. A roadmap for development of neuro-oscillations as translational biomarkers for treatment development in neuropsychopharmacology.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

R E FeatherstoneTranslational Neuroscience Program, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United States.
L R NagyTranslational Neuroscience Program, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United States.
C G HahnMolecular Signaling Program, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United States.
S J SiegelTranslational Neuroscience Program, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United States. Electronic address: siegels@upenn.edu.
University of Pennsylvania · US

Funding

An Implantable Semiannual Antipsychotic Delivery SystemR01MH074672 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI SIEGEL, STEVEN J · 2007 to 2014
$2.3M
Long-term neurobehavioral effects of ketamine exposure in adolescent miceR01DA023210 · NIDA · UNIVERSITY OF PENNSYLVANIA · PI SIEGEL, STEVEN J · 2008 to 2012
$1.9M
NIDA NIH HHS 5R01DA023210-02NIDA NIH HHS R01 DA023210NIMH NIH HHS R01 MH074672
6 · The paper itself

Abstract

backgroundIncreased susceptibility to cognitive impairment or psychosis in adulthood is associated with adolescent drug abuse. Studies in adults have identified impairments in attention and memory, and changes in EEG, as common consequences of ketamine abuse. In contrast, the effects of ketamine on the juvenile brain have not been extensively tested. This is a significant omission, since abuse of ketamine is often observed within this age group.

objectivesJuvenile mice (4-6 weeks of age) were administered ketamine (20mg/kg) for 14 days. EEG was assessed in response to auditory stimulation both at one week following ketamine exposure at 7 weeks of age (juvenile) and again at 12 weeks of age (adult). EEG was analyzed for baseline activity, event-related power and event-related potentials (ERPs).

resultsWhile no effects of ketamine exposure were observed during the juvenile period, significant reductions in amplitude of the P20 ERP component and event-related gamma power were seen following ketamine when re-tested as adults. In contrast, reductions in event-related theta were seen in ketamine-exposed mice at both time points.

conclusionsAge related deficits in electrophysiological components such as P20 or event-related gamma may be due to an interruption of normal neural maturation. Reduction of NMDAR signaling during adolescence leads to delayed-onset disruption of gamma oscillations and the P20 component of the ERP. Further, delayed onset of impairment following adolescent ketamine abuse suggests that methods could be developed to detect and treat the early effects of drug exposure prior to the onset of disability.

Indexed as

Acoustic StimulationAge FactorsAnimalsElectrodes, ImplantedElectroencephalographyEvoked Potentials, AuditoryKetamineMaleMiceMice, Inbred C3HReaction TimeKetamineDrug-abuseGammaNMDAOscillationsSchizophreniaTheta

Identifiers

PMID24210161
PMCPMC4009692
OpenAlexW2015738723

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.